Blood damage safety of prosthetic heart valves. Shear-induced platelet activation and local flow dynamics: a fluid-structure interaction approach.

Thromboembolism and the attendant risk of cardioembolic stroke remains an impediment to the development of prosthetic cardiovascular devices. In particular, altered haemodynamics are implicated in the acute blood cell damage that leads to thromboembolic complications, with platelet activation being the underlying mechanism for cardioemboli formation in blood flow past mechanical heart valves (MHVs) and other blood re-circulating devices. In this work, a new modeling paradigm for evaluating the cardioembolic risk of MHVs is described. In silico fluid-structure interaction (FSI) approach is used for providing a realistic representation of the flow through a bileaflet MHV model, and a Lagrangian analysis is adopted for characterizing the mechanism of mechanically induced activation of platelets by means of a mathematical model for platelet activation state prediction. Additionally, the relationship between the thromboembolic potency of the device and the local flow dynamics is quantified by giving a measure of the role played by the local streamwise and spanwise vorticity components. Our methodology indicates that (i) mechanically induced activation of platelets when passing through the valve is dependent on the phase of the cardiac cycle, where the platelet rate of activation is lower at early systole than late systole; (ii) local spanwise vorticity has greater influence on the activation of platelets (R>or=0.94) than streamwise vorticity (R>or=0.78). In conclusion, an integrated Lagrangian description of key flow characteristics could provide a more complete and quantitative picture of blood flow through MHVs and its potential to activate platelets: the proposed "comprehensive scale" approach could represent an efficient and novel assessment tool for MHV performance and may possibly lead to improved valve designs.

Numerical simulation of the dynamics of a bileaflet prosthetic heart valve using a fluid-structure interaction approach.

The main purpose of this study is to reproduce in silico the dynamics of a bileaflet mechanical heart valve (MHV; St Jude Hemodynamic Plus, 27mm characteristic size) by means of a fully implicit fluid-structure interaction (FSI) method, and experimentally validate the results using an ultrafast cinematographic technique. The computational model was constructed to realistically reproduce the boundary condition (72 beats per minute (bpm), cardiac output 4.5l/min) and the geometry of the experimental setup, including the valve housing and the hinge configuration. The simulation was carried out coupling a commercial computational fluid dynamics (CFD) package based on finite-volume method with user-defined code for solving the structural domain, and exploiting the parallel performance of the whole numerical setup. Outputs are leaflets excursion from opening to closure and the fluid dynamics through the valve. Results put in evidence a favorable comparison between the computed and the experimental data: the model captures the main features of the leaflet motion during the systole. The use of parallel computing drastically limited the computational costs, showing a linear scaling on 16 processors (despite the massive use of user-defined subroutines to manage the FSI process). The favorable agreement obtained between in vitro and in silico results of the leaflet displacements confirms the consistency of the numerical method used, and candidates the application of FSI models to become a major tool to optimize the MHV design and eventually provides useful information to surgeons.

Platelet activation due to hemodynamic shear stresses: damage accumulation model and comparison to in vitro measurements.

The need to optimize the thrombogenic performance of blood recirculating cardiovascular devices, e.g., prosthetic heart valves (PHV) and ventricular assist devices (VAD), is accentuated by the fact that most of them require lifelong anticoagulation therapy that does not eliminate the risk of thromboembolic complications. The formation of thromboemboli in the flow field of these devices is potentiated by contact with foreign surfaces and regional flow phenomena that stimulate blood clotting, especially platelets. With the lack of appropriate methodology, device manufacturers do not specifically optimize for thrombogenic performance. Such optimization can be facilitated by formulating a robust numerical methodology with predictive capabilities of flow-induced platelet activation. In this study, a phenomenological model for platelet cumulative damage, identified by means of genetic algorithms (GAs), was correlated with in vitro experiments conducted in a Hemodynamic Shearing Device (HSD). Platelets were uniformly exposed to flow shear representing the lower end of the stress levels encountered in devices, and platelet activity state (PAS) was measured in response to six dynamic shear stress waveforms representing repeated passages through a device, and correlated to the predictions of the damage accumulation model. Experimental results demonstrated an increase in PAS with a decrease in "relaxation" time between pulses. The model predictions were in very good agreement with the experimental results.